[Effects of hydrogen sulfide preconditioning on myocardial ischemia reperfusion injury in rats].

OBJECTIVE: To investigate the effects of hydrogen sulfide preconditioning on myocardial ischemia reperfusion injury in rats. METHODS: Sprague-Dawley male rats were divided into 4 groups with 10 in each group: in S group rats received sham operation; in IR group rats were given with NS (1.0 ml/kg iv) 24 h before ischemia; in H group rats were treated with NaHS (0.05 mg/kg iv) 24 h before ischemia; and in D group, NaHS-treated rats received 5-hydroxydecanoate (5-HD) 15 min before ischemia. Rats in IR group,H group and D group were subjected to ischemia by occlusion of coronary artery for 30 min followed by 2 h of reperfusion. At the end of the reperfusion,myocardial infarct size was measured. SAM-s was measured by Western blotting. Plasma SOD activity and MDA were determined at the end of reperfusion. RESULTS: The infarct size was significantly lesser in H group (25.40 % ± 3.54%) than that in IR group (38.27% ±5.64%,P<0.05). The SAM-s protein expression in myocardium was significantly lower in H group than that in IR group. The plasma MDA content was significantly lower and SOD activity was higher in H group than those in IR group,but there was no difference between IR group and D group. CONCLUSION: The hydrogen sulfide preconditioning attenuates myocardial IR injury possibly through down-regulating SAM-s expression,reducing the production of oxygen free radicals and enhancing anti-oxidize effect in rats.

[Proteomics analysis of myocardium after delayed preconditioning with hydrogen sulfide in rat].

OBJECTIVE: To investigate the changes in protein of myocardium after hydrogen sulfide delayed preconditioning by using proteomics technology. METHODS: Sixteen Sprague-Dawley rats were randomly assigned to control (group S) or hydrogen sulfide group (group H), n = 8 for each group. Myocardial ischemia/reperfusion injury model (ischemia 30 minutes followed by reperfusion 120 minutes) was reproduced at 24 hours after preconditioning either with normal saline or hydrogen sulfide for proteomics analysis in group S or group H, and the myocardial tissue was harvested. The total proteins were extracted and separated by two dimensional gel electrophoresis (2-DE), and the differential protein expression spots were analyzed with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). RESULTS: Analysis of 2-DE showed that 929 ± 14 protein spots were found in group S and 906 ± 10 protein spots in group H, and the expression of 15 protein spots was different between two groups. These protein spots were chosen to undergo MALDI-TOF-MS analysis, and 11 proteins were preliminarily identified, including DNA ligase, cystathionine gamma-lyase, transcription initiation factor, NADH dehydrogenase, guanine nucleotide-releasing factor, fructose-bisphosphate aldolase A, glycogen synthase kinase-3, electron transfer flavoprotein subunit beta, glutathione S-transferase, soluble calcium-activated nucleotidase and S-adenosylmethionine synthetase. CONCLUSIONS: Hydrogen sulfide delayed preconditioning of myocardium resulted in the changes in protein expression profiles in the myocardium. The differential proteins might function as anti-oxidants, to improve the energy metabolism of myocardium, confer cytoprotection and protection of respiratory chain, thus conferring cardioprotection.

[Effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase expression during myocardial ischemia-reperfusion in rats].

OBJECTIVE: To investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats. METHODS: Sprague-Dawley male rats were randomly divided into 4 groups (n= 10 in each): Group S (sham operation group), Group IR (ischemia/reperfusion group), Group H (IR+ NaHS 0.05 mg/kg iv, 24 h before ischemia) and Groups D receiving IR+NaHS 24 h before ischemia and 5-hydroxydecanoate (5-HD)15 min before ischemia. Animals in groups IR, H and D were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS) was examined. Glutathione S-transferase (GST) was measured by Western blotting. The myocardial ultrastructures were observed under the electron microscopy. RESULTS: The IS was significantly smaller in Group H than that in Group IR [(25.40 ± 3.54)% compared with (38.27 ± 5.64)%, P<0.05]. The GST expression in myocardium was significantly higher in Group H than that in Group IR. Microscopic examination showed less myocardial damage in Group H than in Group IR. The protective effects of delayed preconditioning by hydrogen sulfide was prevented by 5-HD pre-treatment. CONCLUSION: The hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats.

Delayed preconditioning by sevoflurane elicits changes in the mitochondrial proteome in ischemia-reperfused rat hearts.

BACKGROUND: Delayed myocardial preconditioning by volatile anesthetics involves changes in DNA transcription and translation. Mitochondria play a central role in myocardial ischemia/reperfusion (I/R) injury and in ischemic or pharmacologic preconditioning. In this study, we investigated whether there are alterations in myocardial mitochondrial protein expression after volatile anesthetic preconditioning (APC) to examine the underlying mechanisms of delayed cardioprotection. METHODS: Thirty-six Sprague-Dawley rats were randomly assigned to 1 of 3 groups (n = 12 for each group). Rats in the delayed APC group were exposed to sevoflurane (2.5% for 60 minutes) 24 hours before myocardial ischemia was induced. Myocardial ischemia in the I/R and APC groups was induced by left coronary artery occlusion for 30 minutes, followed by 120 minutes of reperfusion. The control group received no treatment. The mitochondria fractions were prepared by differential centrifugation with density gradient isolation for proteomic analysis. Two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization with time-of-flight mass spectrometry was used to identify differences in the protein expression from mitochondria of the rat hearts. RESULTS: Fifteen differentially expressed mitochondrial proteins between the APC group and I/R group were identified and the expression patterns of 2 of the proteins were confirmed by Western blot analysis. These proteins were associated with mitochondrial substrate metabolism, respiration, and adenosine triphosphate (ATP)/adenosine diphosphate transport. The modifications of the mitochondrial proteome suggest an enhanced capacity of mitochondria to maintain myocardial ATP levels after I/R injury. CONCLUSION: Delayed sevoflurane myocardial preconditioning induces mitochondrial proteome remodeling, which mainly involves proteins that are related to ATP generation and transport. Therefore, proteomic changes related to bioenergetic balance may be the mechanistic basis of delayed anesthetic myocardial preconditioning.

[Effect of morphine postconditioning on myocardial ischemia-reperfusion injury in rabbits].

OBJECTIVE: To investigate the protective effects of morphine postconditioning on myocardial ischemia-reperfusion (I/R)injury and the potential mechanisms in rabbits. METHODS: Thirty-two New Zealand male white rabbits were randomly assigned into 4 groups: Group 1 (Sham), Group 2 (I/R), Group 3 (ischemic postconditioning), Group 4 (ischemia and morphine postconditioning). Group 1 was perfused for 160 min; Group 2 underwent 40 min ischemia and 120 min reperfusion; Group 3 underwent three cycles of 30 s reperfusion and 30 s left anterior descending coronary artery re-occlusion immediately after 40 min ischemia and before 120 min reperfusion; Group 4 was given morphine 1.0 mg/kg immediately after 40 min ischemia in 1 min and before 120 min reperfusion. Blood samples were taken from arterial line at 20 min before occlusion, 20 min after occlusion, 40 min after occlusion, 1 h after reperfusion and 2 h after reperfusion for determination of the plasma levels of cardiac troponin I (cTnI). At the end of the reperfusion, infarct size (IS) and area at risk were defined by Evans and TTC staining. Plasma SOD activity and MDA were determined at the end of reperfusion. RESULT: The levels of cTnI were significantly lower during reperfusion in the two postconditioning groups than those in I/R group. The plasma MDA content was significantly lower and SOD activity was significantly higher in the two postconditioning groups than those in I/R group, but there was no difference between two postconditioning groups. Morphine significantly reduced infarct size of the left ventricular area at risk as compared with I/R group (P<0.05). CONCLUSION: Morphine postconditioning is as effective as ischemic postconditioning in the protection of myocardium against I/R injury in rabbits. Decrease in oxygen free radicals and increased antioxidant activity might be involved in its mechanism.

[Preconditioning of morphine protects rabbit myocardium from ischemia-reperfusion injury].

OBJECTIVE: To investigate the protective effects of preconditioning morphine on rabbit myocardium during ischemia-reperfusion. METHODS: Thirty New Zealand male white rabbits were randomly assigned to three groups: control, I/R and morphine groups. In morphine group 1.0 mg/kg morphine was given preoperationaly, in control and I/R groups 1.0 ml/kg NS was given. Twenty-four hours later rabbits in morphine and I/R groups underwent 40 min of coronary occlusion followed by 2 hours of reperfusion; for control group only sham operation was performed. At the end of the reperfusion, infarct size (IS) and area at risk (AAR) were defined by Evans blue and TTC staining. At the end of the reperfusion blood samples were taken for determination of plasma SOD activity and MDA levels. The heart was harvested and levels of the HSP27 were determined by Western blot, and the heart ultrastructures were observed under the electron microscopy. RESULTS: Compared with I/R group,morphine significantly reduced infarct size (21.5%+/-2.4% Compared with 37.8%+/-1.7%, P<0.05). The morphine had a lower level of MDA and higher levels of SOD and HSP27 than those in I/R. CONCLUSION: Preconditioning of morphine demonstrates cardioprotective effect on ischemia/reperfusion injury, which may be associated with increased HSP27 levels in the heart.

[Effect of fructose-1,6-diphosphete on myocardial preservation during pulmonary operations].

OBJECTIVE: To investigate the effect of fructose-1,6-diphosphete(FDP) on myocardial preservation in pulmonary operations. METHODS: One hundred and six patients undergoing selective pulmonary lobectomy or segmentectomy were randomly divided into 2 groups with 53 patients each. FDP 200 mg/kg was infused intravenously before anesthesia in the FDP group, while 5% glucose with the same volume was given instead of FDP in the control group. ECGs were monitored from before the anesthesia to 72 h after the operation;the time and type of arrhythmia were recorded. Blood samples were taken before the operation (T0), immediately after the operation(T1), at 24 h(T2),48 h(T3)and 72 h(T(4)) after the operation to determine plasma creatine kinase isoenzyme MB(CK-MB) and cardiac troponin I(cTnI) concentrations. RESULTS: The incidence of arrhythmia in FDP group (35 times) was significantly lower than that in the control group(67 times). The incidence of all types of arrhythmia in the FDP group was also significantly lower than that in the control group. The concentrations of CK-MB and cTnI in the FDP group were significantly lower than those in the control group at T1, T2, T3, and T4. CONCLUSION: FDP is effective for myocardial preservation in pulmonary operations.

[Effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury in rabbits].

OBJECTIVE: To investigate the protective effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury and the potential mechanism in rabbits. METHODS: Thirty New Zealand male white rabbits were randomly assigned to 3 groups: Control group; I/R group; and 2.0% isoflurane group. Isoflurane group was exposed to 2.0% isoflurane-100% oxygen for 2 hours. Control group and I/R group were exposed to 100% oxygen for 2 hours and served as untreated controls. Twenty-four hours later I/R group and isoflurane group underwent 40 minutes of coronary occlusion followed by 2 hours of reperfusion. Blood samples were taken from the arterial line at 20 minutes before the occlusion(T1), 20 minutes after the occlusion(T2), 40 minutes after the occlusion(T3), 1 hours after the reperfusion(T4), and 2 hours after the reperfusion(T5) to determine the plasma level of TNF-alpha. At the end of the reperfusion, infarct size and area at risk were defined by Evans and TTC staining. The heart was harvested and levels of the p38MAPK activity were determined by Western blot, and ultrastructures were observed under the electron microscope. RESULTS: The p38MAPK activity of isoflurane group was significantly lower than that of I/R group (P<0.05). Isoflurane significantly (P<0.05) reduced the infarct size(19.7%+/-2.8% in isoflurane group) of the left ventricular area at risk as compared with the controls (37.8%+/-1.7% in I/R group).The injury of I/R group was worse than that of isoflurane group under the light microscope. Isoflurane group had a lower level of TNF-alpha than I/R group. CONCLUSION: Isoflurane can inhibit p38MAPK activity during myocardial ischemia reperfusion and modulate the cytokine expression, which may be one of the molecular mechanisms of isoflurane delayed preconditioning on cardioprotection.

[Protective effect of heat-shock protein 27 on myocardium with isoflurane preconditioning in myocardial ischemia/reperfusion injury of myocardium in rabbit].

OBJECTIVE: To investigate the mechanism and the protective effect of heart-shock protein 27 (HSP27) on rabbit myocardium with isoflurane preconditioning in myocardial ischemia/reperfusion (I/R) injury. METHODS: Thirty New Zealand white rabbits were randomly assigned to three groups (each n = 10):(1)Sham operation group (C group); (2)I/R group; (3)Two percent in volume is of isoflurane group (S group). S group was exposed to 2.0% isoflurane-pure oxygen for 2 hours. C group and I/R group were exposed 2 hours to pure oxygen to serve as untreated controls. Twenty-four hours later the rats in I/R group and S group underwent 40 minutes of coronary occlusion followed by 120 minutes of reperfusion. At the end of the reperfusion, infarct size (IS) was defined by Evan's blue and triphenyltetrazolium chloride (TTC) staining. Blood samples were taken from arterial line for determination of malondialdehyde (MDA) levels. Western Blotting was used to determine the expression of HSP27 and nuclear factor-KappaB (NF-KappaB) in myocardium. RESULTS: Isoflurane preconditioning could decrease I/R induced myocardial infarct size [(19.7 +/- 2.8)% vs.(37.8 +/- 1.7)%]. This was accompanied by an increase in the expression in HSP27 [(84.5 +/- 4.3) gray scale value vs. (53.1 +/- 3.8) gray scale value] and a decrease in NF-KappaB [(58.6 +/- 4.2) gray scale value vs. (119.3+/-5.6) gray scale value] and MDA [(5.24 +/- 0.45)kU/L vs. (9.42 +/- 0.83)kU/L]. CONCLUSION: The expression of HSP27 induced by isoflurane preconditioning plays an important role in protecting myocardium against ischemia/reperfusion injury.

[Effect of morphine on dorsal horn projection neurons in neuropathic pain rats].

OBJECTIVE: To explore the inhibitory effect of spinal topical morphine on the dorsal horn projection neurons in nerve-injured rats and its mechanism. METHODS: Single-unit activity of dorsal horn projection neurons was recorded in anesthetized L(5)/L(6) nerve-ligated rats. Allodynia was determined by a behavior test in nerve-injured rats. The evoked neuronal responses to mechanical stimuli applied to the receptive field were determined before and after the spinal topical application of morphine, bicuculline plus morphine, strychnine plus morphine, and both bicuculline and strychnine plus morphine in normal, sham operation, and nerve-injured rats. RESULTS: Spinal topical application of 10 micromol/L morphine significantly inhibited the evoked responses of dorsal horn projection neurons in normal, sham, operation and nerve-injured rats. However, the inhibitory effect of morphine was significantly reduced in nerve-injured rats compared with that in normal and sham operation rats. Furthermore, the topical application of 20 micromol/L bicuculline had little effect on the inhibitory effect of morphine in nerve-injured rats but it almost abolished the effect of morphine in normal and sham operation rats. The glycine receptor antagonist strychnine at 4 micromol/L significantly decreased the effect of morphine in nerve-injured, normal, and sham operation rats. CONCLUSION: The loss of tonic GABAergic inhibition contributes to the reduced inhibitory effect of morphine on dorsal horn projection neurons in nerve-injured rats.

[Effect of chloroquine on the apoptosis of intestinal mucosa epithelial cells and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats].

OBJECTIVE: To observe the effect of chloroquine on the apoptosis of intestinal mucosa epithelial cell and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats. METHODS: The rat total hepatic ischemia-reperfusion model was built by blocking the hepatic portal, suprahepatic and infrahepatic vena cava for 20 minutes. Ninety Sprague-Dawley rats were assigned randomly into the sham operation group (Group A, n = 30), total hepatic ischemia-reperfusion treatment group (Group B, n = 30), and chloroquine administrated group (Group C, n = 30). Each group was subdivided randomly into 3 subgroups (n = 10) according to different experiment time phases as follows: after 20 minutes of total hepatic vascular exclusion (T0), 4 hours after reperfusion (T1), and the 48 hours of survival. Group A and Group B were intravenously injected with normal saline 1 mL/kg while Group C received chloroquine 10 mg/kg which dissolved in 1 mL/kg normal saline intravenously. The levels of portal blood D-lactate, TNF-alpha, endotoxin, and the intestinal mucosa MDA concentration were measured at T0 and T1; the portal blood, mesenteric lymph node, and spleen tissues were cultured for bacteria; and the apoptotic index of intestinal mucosa epithelial cells at T0 and T1 and the survival rate after 48 hour reperfusion were obtained. RESULTS: Compared with Group A, the levels of portal blood D-lactate, TNF-alpha, endotoxin and the intestinal mucosa MDA in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). These indexes of Group C were lower than those of Group B (P < 0.05). The portal vein blood, mesenteric lymph node and spleen tissues existed the bacterium translocation both in Group B and Group C, and the positive rate in Group C was lower than that in Group B (P < 0.05). Apoptotic index of the intestinal mucosa epithelial cell increased significantly in Group B (P < 0.01) and Group C (P < 0.05), but the apoptotic index in Group C was lower than that in Group B (P < 0.05); the 48 hour survival rate of the rats in Group C was higher than that in group B (P < 0.05). CONCLUSION: Chloroquine may decrease the intestinal mucosa epithelial cell apoptosis and the enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion and increase the survival rate of the rats.

[Effects of different doses of fentanyl on the stress response in patients undergoing valve replacement].

OBJECTIVE: To investigate the effects of different doses of fentanyl on the stress response in valve replacement surgery during cardiopulmonary bypass (CPB). METHODS: Thirty ASA II-III adult patients scheduled for cardial valve replacement were randomly divided into 3 groups: Group A (fentanyl 30 microg/kg), Group B (fentanyl 60 microg/kg), and Group C (fentanyl 100 microg/kg). Anesthesia was induced with medazalam 0.1 mg/kg, fentanyl 10 microg/kg and vecuronium 0.1 mg/kg; And were maintained with fentanyl and propofol infusion. Remained dose of fentanyl was used before the CPB. MAP, CVP, HR, P(ET)CO2, SpO2, nasal and rectal temperature were monitored continuously. Blood samples were taken before the operation (T1), before the CPB (T2), 30 min after the aortic declamping (T3), 2 h after the aortic declamping (T4), 24 h (T5) after the operation to determine the plasma levels of glucose, adrenocorticotropic hormone (ACTH), angiotensin II (AT II) and cortisol. RESULTS: Levels of glucose, ACTH, AT II and cortisol after the CPB (T3, T4 and T5) in 3 groups were significantly increased compared with that of T1 (P < 0.05 or P < 0.01). After CPB, at the same time point, among the 3 groups, the levels of the above index of Group A were the most highest, that of Group C were the most lowest. Glucose, ACTH, AT II and cortisol levels at T3 and T4 were significantly lower in Group B and C than those in Group A ( P < 0.05); But there was no significant difference between Group B and C. The duration of stay in the ICU and time of endotracheal extubation were significantly longer in patients of Group C than Group A and B (P < 0.05). CONCLUSION: Fentanyl (30-100 microg/kg) can completely suppress the stress response induced by intubation and intense surgical stimulus before CPB. Different doses of fentanyl seemed to be effective in reducing CPB-induced stress response. But the effect was not dependent on dose. So 60 microg/kg fentanyl seemed to be an ideal dose.

[Effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats].

OBJECTIVE: To investigate the effects of aminoguanidine on the lung injury induced by the total hepatic ischemia-reperfusion in rats. METHODS: The total hepatic ischemia-reperfusion model was built after blocking of the hepatic porta, suprahepatic and infrahepatic vena cava. Ninety Sprague-Dawley rats were assigned randomly into 3 groups: Sham operation group (Group A, n=30); total hepatic ischemia group (Group B, n=30); and aminoguanidine treatment group (Group C, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different time phases: 20 minutes after the total hepatic vascular exclusion (T0), 4 hours after the reperfusion (T1), and 48 hours after the survival Group A and Group B were intravenously injected with normal saline ( mL/kg) while Group C was injected with aminoguanidine (20 mg/kg) dissolved in normal saline (1 mL/kg) 10 minutes before the open of the abdomin. The levels of portal blood nitric oxide ( O) endotoxin ( ET), tumor necrosis factor-alpha (TNF-alpha at T0 and T1 were detected; 48 hours survival rates and the lung wet/dry weight ratio were counted; and the histological changes of the lung tissues were observed. RESULTS: Compared with Group A, the levels of portal vein NO, ET, and TNF-alpha T0 and T1 in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). But those indexes of Group C were lower than those of Group B (P < 0.05). The 48-hour survival rate in Group C was higher than that in Group B (P < 0.05). The lung wet/dry weight ratio in Group C was lower than in Group B (P < 0.05) and the histological change of Group C was slighter than that in Group B. CONCLUSION: Aminoguanidine has the protective effects on the lungs against the total hepatic ischemia-reperfusion induced injury.

[Effects of ulinastatin on cerebral inflammatory response during cardiopulmonary bypass].

OBJECTIVE: To investigate the effects of ulinastatin (UTI) on cerebral inflammatory response during cardiopulmonary bypass (CPB). METHODS: Twenty-four NYHA II-III patients (13 males and 11 females) aged 23-45 years, undergoing elective cardiac valve replacement under hypothermic CPB were randomly divided into 2 groups: ulinastatin group (Group U, n=12) and control group (Group C, n=12). In group U, UTI (1.2 x 10(4) U/kg) was given intravenously after the induction of anesthesia, 0.6 x 10(4) U/kg UTI was added to the priming solution, and 0.6 x 10(4) U/kg UTI was given about 5 min before the aortic decamping. In Group C, normal saline was given instead of UTI. Internal jugular vein was cannulated and the catheter was advanced retrogradely till jugular bulb. Blood samples were taken simultaneously from artery and jugular bulb after induction of anesthesia (T1), 60 min (T2) and 6 h (T3) after discontinuation of CPB for determination of TNFalpha, IL-6, IL-8 and IL-10. The juguloarterial gradients of these cytokines (deltaTNFalpha, deltaIL-6, deltaIL-8, and deltaIL-10) were calculated. RESULTS: In Group C, arterial levels of TNFalpha, IL-6, IL-8, IL-10 at T2 and T3, deltaTNFalpha, deltaIL-8 and deltaIL-10 at T2, deltaTNFalpha, deltaIL-6 and deltaIL-10 at T3 significantly increased (P < 0.01). deltaIL-8 increased at T3 (P < 0.05). In Group U, arterial levels of IL-6, IL-8, IL-10 at T2, arterial levels of IL-6, IL-8,IL-L-10 and deltaTNFalpha, deltaIL-8 at T3 significantly increased (P < 0.01). Arterial levels of TNFalpha at T2 and T3, deltaTNFalpha, deltaIL-10 at T2, deltaIL-6 at T3 increased (P < 0.05). Arterial levels of TNFalpha, IL-6 and deltaTNFalpha, deltaIL-8 at T2, arterial levels of TNFalpha and deltaIL-6 at T3 in Group U were lower than those in Group C (P < 0.05). Arterial levels of IL-6 at T3, IL-8 at T2 and T3 in Group U were significantly lower than those in Group C (P < 0.01). Arterial levels of IL-10 and deltaIL-10 at T3 in Group U were higher than those in Group C (P < 0.05). CONCLUSION: Systemic and cerebral activation of inflammatory response during CPB can be alleviated by ulinastatin.

[Treatment with total hepatic vascular exclusion and reperfusion for the intestinal barrier in rats].

OBJECTIVE: To investigate the influence of treatment with total hepatic vascular exclusion and reperfusion on the intestinal barrier in rats. METHODS: The total hepatic vascular exclusion and reperfusion model was built after the block of hepatic portal, suprahepatic and infraheptic vena cava for 20 minutes. Sixty Sprague-Dawley rats were divided randomly into 2 groups: sham operation group (Group A, n=30) and total hepatic vascular exclusion and reperfusion treatment group (Group B, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different experiment time points as follows: at the end of the total hepatic vascular exclusion (T0), 4 reperfusion after total hepatic vascular exclusion (T1) and the 48 h survival. Portal vein blood gas was analysed at T0. At T0 and T1 the following items were detected: the level of portal vein blood D-lactate, tumor necrosis factor-alpha (TNF-alpha), the MDA concentration and pathologic morphology change of intestinal mucosa. RESULTS: Compared with Group A, the PCO2 at T0 in Group B increased while pH, P02, and HCO3- decreased significantly (P < 0.05). The level of portal blood D-lactate, TNF-alpha and intestinal mucosa MDA at T0 and T1 was significantly higher (P < 0.05, or P < 0.01). The histologic damage in the intestinal mucosa was observed in Group B, and the rat survival in Group B was lower than that in Group A (P < 0.05). CONCLUSION: The treatment with total hepatic vascular exclusion and reperfusion can damage the intestinal barrier in rats.

[Effects of fentanyl on cytokines and MDA during cardiopulmonary bypass in patients undergoing valve replacement].

OBJECTIVE: To investigate the effect of fentanyl on cytokines and MDA in valve replacement surgery during cardiopulmonary bypass ( CPB). METHODS: Thirty ASA II approximately III adult patients scheduled for cardial valve replacement were randomly divided into 3 groups: Group A (fentanyl 30 microg/ kg), Group B (fentanyl 60 microg/kg), and Group C (fentanyl 100 microg/kg). Anesthesia was induced with medazalam 0.1 mg/kg, fentanyl 10 microg/kg and vecuronium 0.1 mg/kg Administered intravenously. After tracheal intubation the patients were mechanically ventilated with pure oxygen. P(ET)CO2 was maintained between 35 approximately 45 mmHg. Anesthesia were maintained with fentanyl infusion combined with intermittent intravenous bolus of midazolam and vecuronium. MAP, CVP, HR, P(ET)CO2, SPO2, nasal and rectal temperature were monitored continuously. Remained dose of fentanyl was infused before the CPB. Blood Samples were taken before the operation (T1 ), before the CPB ( T2 ), 30 min after aortic declamping (T3 ) , 2 h after aortic declamping (T4 ), and 24 h (T5 ) after the operation for determination of plasma levels of tumor necrosis factor (TNF-alpha), interteukin IL-6 and IL-10, MDA. RESULTS: There was no significant change in the age, body weight, aortic cross-clomp time, CPB time, and operation time. Levels of TNF-alpha, IL-6, IL-10 and MDA after the CPB in the 3 groups were significantly higher compared with T, (P <0.01 ), TNF-alpha, IL-6 and MDA levels at T3, T4 were significantly lower in Group B and C than those in Group A. IL-10 levels at T4, T5 were significantly higher in Group B and C than those in Group A, but levels of TNF-alpha, IL-6, IL-10 and MDA in Group B were not significantly different compared with those in Group C. The duration of stay in the ICU and time of endotracheal extubation were significantly longer in patients of Group C than those of Group A and B. CONCLUSION: CPB leads to a proinflammatory and antiinflammatory response, as well as oxygen free radicals release. Larger dose fentanyl seemed to be effective in reducing CPB-induced inflammatory response and ischemic reperfusion injury, but the effect was not dependent on dose while fentanyl dose reaching some value, at the same time the duration of stay in ICU and time of endotracheal extubation is longer.